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Biomedical subjects

O Johansen

Publications and source records attributed to O Johansen.

At least 19 recordsLinked to original sources
PubMed1995

The effects of 'in-use' surgical handwashing on the pre- and postoperative fingertip flora during cardiothoracic and orthopaedic surgery.

Two operating teams (25 persons) were followed for two months with fingerprint samples taken preoperatively; before and after 'in-use' surgical handwashing; and immediately postoperatively, with and without surgical gloves. The mean time for handwashing for the cardiothoracic team (CT) was 2 min and for the orthopaedic team (OT) was 3.5 min. A closer observation of 10 persons revealed a great individual variation in washing techniques, in spite of standard guidelines. The CT team performed eight, and the OT team nine sterile operations with an average duration of 3 h and 20 min and 2 h and 40 min, respectively. Surgical handwashing resulted in fingertip sterility in 111/118 (94.1%) cases; in 61/66 (92.4%) samples from the surgeons and in 50/52 (96.2%) samples from the assistants. Postoperative fingerprinting with gloves on showed sterile conditions in 85/91 (93.4%) samples; 57/59 (96.6%) from the surgeons and 28/32 (87.5%) from the assistants. Immediately after removal of the gloves, 43/67 (64.2%) of fingerprint samples from the surgeons and 13/48 (27.1%) from the assistants were still sterile. Coagulase-negative staphylococci (CNS) and Bacillus species predominated in fingerprint samples. Of the 105 CNS strains tested, 11.4% were methicillin resistant. Only five strains of Staphylococcus aureus were isolated; in 4/5 cases from the OT. This study illustrates that in spite of standard guidelines, there is great individual variation in surgical handwashing. However, in most instances, the bacteria are eradicated from the fingertips. Even after surgery for 2-3 h, there may still be a residual effect of the hand disinfecting agent in half of the cases.

Bacteria↗
PubMed1995

Effects of naloxone on glucagon and insulin concentrations after injection of endotoxin in rats.

OBJECTIVE: To find out how infusions of endotoxin and endotoxin plus naloxone affected glucose, glucagon, and insulin concentrations in rats. DESIGN: Random control study. SETTING: University hospital, Norway. MATERIAL: 27 Male Wistar rats. INTERVENTIONS: 8 Rats were given Escherichia coli endotoxin 0.25 mg in saline; 5 were given a naloxone infusion (0.4 ml of 0.04 mg/ml for the first half hour and continued at a rate of 0.4 ml/hour for a total of 80 minutes) starting 10 minutes before the same dose of endotoxin; 6 were given saline alone for 70 minutes, and 8 saline alone for 10 minutes. Blood was taken for analysis after 70 minutes in the first three groups and at the end of the infusion in the 10 minute group. MAIN OUTCOME MEASURES: Serum concentrations of glucose, glucagon, and insulin compared with baseline (10 min group). RESULTS: Median (interquartile) concentrations of all three substances rose significantly 70 minutes after the injection of endotoxin compared to basal values: 9.8 (8.2-10.9) compared with 6.0 (4.8-7.5) mmol/l for glucose (p < 0.01); 53.1 (44.6-56.0) compared with 3.6 (3.1-5.1) ng/l for glucagon; and 39.4 (38-50.4) compared with 16.7 (11.2-25.5) pmol/l for insulin. When naloxone was combined with endotoxin glucagon and insulin concentrations were significantly lower: 24.3 (23.9-37.5) ng/l (p < 0.01), and 30.6 (24.5-31.6 pmol/l (p < 0.05), respectively. The concentration of glucose in venous blood was unchanged. CONCLUSIONS: The rise in glucagon and insulin concentrations after endotoxin infusions may be partly mediated by opioids. Naloxone in the dose given did not abolish the increase in glucagon after endotoxin. The high glucagon:insulin ratio after both endotoxin alone and endotoxin plus naloxone may be important in the aetiology of the hyperglycaemia seen.

Animals↗
PubMed1994

[Stress echocardiography with dobutamine. A new method for diagnosis of ischemia].

Dobutamine stress echocardiography was performed in 24 patients with angiographically defined coronary artery stenosis, before they underwent percutaneous transluminal coronary angioplasty. Ischemia was detected on stress-ECG in 13 patients. In 19 patients ischemia could be detected with dobutamine stress echocardiography. The method was highly sensitive for detecting ischemia in patients with two vessel or three vessel disease and in patients with affection of only the left anterior descending artery. In patients with one vessel disease the method showed low sensitivity. The most common side effects of dobutamine infusion were flushing and palpitations. One patient suffered atrial fibrillation and one patient had a short and self-limiting ventricular tachycardia. The method seems to be a useful and safe supplementary tool for detecting myocardial ischemia. It is also useful for characterizing the physiological effect of coronary artery stenosis.

Coronary Disease↗
PubMed1994

Morphine effects on the release of glucagon, insulin and somatostatin from the isolated, perfused rat pancreas.

The pancreatic glands from six male Wistar rats weighing between 200 and 250 g were isolated and perfused. After 30-min equilibration and 20-min basal periods, perfusion with 0.2 mg/ml of morphine for 20 min resulted in a significant (P < 0.05) increase in insulin release, with no changes in release of gucagon or somatostatin. After a recovery period of 20 min, a higher morphine concentration of 2 mg/ml was introduced for another 20-min period. With this morphine dose there were significant increases in release of insulin (P < 0.05), glucagon (P < 0.01) and somatostatin (P < 0.05). This shows that morphine induces the release of insulin, glucagon and somatostatin from pancreas in a dose-dependent way, and that release of insulin and glucagon is not primarily affected by regulation of somatostatin levels.

Animals↗
PubMed1994

Increased plasma glucose levels after Hypnorm anaesthesia, but not after Pentobarbital anaesthesia in rats.

The effects of the fentanyl fluanisone combination (Hypnorm) and pentobarbitone sodium (Pentobarbital) anaesthesia on blood glucose, insulin and glucagon were tested in rats in the fed and fasted state. Blood glucose was measured before and at 10, 20 and 30 min after injection of the anaesthetic agents. At 30 min the rats were sacrificed, and blood was drawn for measurement of glucagon and insulin. Pre-anaesthetic values for insulin and glucagon were established in separate groups of fasted and fed rats. In fasting rats given Hypnorm, blood glucose and plasma insulin were unchanged while there was a non-significant increase in plasma glucagon. The fasted rats given Pentobarbital had unchanged blood glucose and plasma insulin and a non-significant depression of glucagon. The fed rats given Hypnorm had a significant increase in blood glucose at 10 min and nearly a doubling of glucose values at 20 and 30 min (P < 0.001). Glucagon increased far less than in the fasted group, whereas insulin was doubled from preanaesthetic values (P < 0.05). The fed rats given Pentobarbital, had unchanged blood glucose, a slight non-significant depression of glucagon and a significant increase in insulin (P < 0.01). Thus Hypnorm induced hyperglycaemia in fed but not in fasted rats, probably because more glucose was available in the fed state. Fed animals are a modification of the standard fasted animal model, and may be preferable when exploring hyperglycaemic or other reactions to anaesthetic agents.

Anesthesia↗
PubMed1994

Haemorrhage-induced increases in glucose, glucagon and insulin levels are blocked by naloxone in rats.

OBJECTIVE: To find out if the opioids that are liberated during bleeding influence the concentrations of glucagon, insulin, somatostatin, corticosterone and glucose in rats, and if naloxone has any regulatory effect. DESIGN: Laboratory study. SETTING: University hospital. MATERIAL: 56 Male Wistar rats. INTERVENTIONS: Removal of blood corresponding to 2% of body weight through a catheter in the internal jugular vein. Before bleeding (n = 8), and at 5, 15 and 30 minutes afterwards (n = 16 at each time point, half of which had received naloxone 0.04 mg/ml, 0.7 ml/hour, for 10 minutes before bleeding and up to 30 minutes afterwards) rats were killed and samples of heart blood taken. MAIN OUTCOME MEASURES: Concentrations of glucose, glucagon, insulin, somatostatin, and corticosterone in heart blood. RESULTS: In the control group (saline) concentrations of glucose, glucagon and insulin increased significantly after bleeding, and had returned to baseline concentration by 30 minutes. Naloxone blocked the increases in the treated group. CONCLUSION: Endogenous opioids, possibly endorphin, may be important in the acute regulation of blood glucose, glucagon and insulin concentrations after haemorrhage.

Animals↗
PubMed1993

Comparison of the modifying effects of somatostatin and propranolol on morphine-induced changes in glucose, glucagon and insulin levels in fed rats.

Twenty-eight rats in four different groups were used. Catheters were implanted in the carotid artery and jugular vein one week before the experiments were performed. The rats were trained to the experimental situation daily, and allowed food and water ad libitum. One group of rats was used to establish control values; a second was injected with morphine (10 mg/ml, 1 ml/kg); a third group got morphine injection (10 mg/ml, 1 ml/kg) combined with somatostatin infusion (0.01 mg/ml, 1 ml/h); and the fourth group was injected with morphine (10 mg/ml, 1 ml/kg) combined with propranolol (0.4 ml, 1 mg/ml). Blood samples for venous glucose and arterial insulin and glucagon were drawn 15 min after start of stimulation. Glucose, insulin and glucagon levels were significantly higher in morphine treated than in control rats. When morphine was combined with somatostatin, the increase in glucose, insulin and glucagon was significantly reduced. However, after the morphine and propranolol stimulation the increase in glucose and glucagon was significantly reduced, whereas the insulin levels were as high as when morphine was given alone. The combined reduction of both glucagon and glucose after somatostatin or propranolol treatment in morphine exposed rats, points to glucagon as a potential link between opioid stimulation and hyperglycemia. Beta-receptor stimulation seems to contribute to the glucagon but not to the insulin release after morphine.

Animals↗
PubMed1993

Morphine and morphine/naloxone modification of glucose, glucagon and insulin levels in fasted and fed rats.

In rats weighing 200-250 g catheters were placed in the internal jugular vein and carotid artery. After 1 week of accommodation the training for the experimental situation, morphine (10 mg kg-1) was injected intravenously alone or in combination with naloxone (0.04 mg ml-1, 0.8 ml h-1). Otherwise no form of anaesthesia was used during the experiments. In control fed and fasted rats, there were no significant differences in blood glucose. In fed rats, morphine increased blood glucose as compared to control rats (p < 0.001). This was not seen in the fasted rats. The morphine induced increase in blood glucose in the fed rats was abolished by naloxone (p < 0.001). Glucagon was significantly higher in fasted than in fed control rats (p < 0.01). It was significantly increased after morphine in fed (p < 0.05), but not in fasted rats. The morphine induced increase in glucagon in fed rats was abolished by naloxone (p < 0.01). Insulin was significantly higher in fed than in fasted control rats (p < 0.05). Morphine increased insulin levels significantly in fed and fasted rats (p < 0.001), p < 0.01). The morphine induced increase in insulin in the fed rats was abolished by naloxone treatment. It is concluded that morphine stimulates glucose and glucagon release in fed but not fasted rats, and that these increases are caused by opioid action. Insulin increases after morphine were proved to be opioid-mediated only in the fed state.

Animals↗
PubMed1992

Increments in glucose, glucagon and insulin after morphine in rats, and naloxone blocking of this effect.

In awake rats adapted to experimental conditions and allowed food ad libitum, hyperglycemia was induced by the administration of morphine 10 mg/kg through indwelling catheters in the external jugular vein. High glucose values were measured at 5, 15 and 25 min. Glucagon values were high at 5 and 15 min, and again at basal level at 25 min. Insulin was increased after morphine both at 5, 15 and 25 min, whereas somatostatin levels did not change after morphine. When morphine was administered together with naloxone after an initial 10 min period of naloxone administration, there was no increment in glucose, insulin or somatostatin values; neither at 5, 15 or 25 min. There was a remarkable glucagon decrease after naloxone and morphine remaining from 5 to 25 min. Then, one of the possible mechanisms for the hyperglycemic response after morphine may be an opioid effect on pancreas, stimulating glucagon and thereby causing hepatic glucose output.

Animals↗
PubMed1990

[Birger Malling's pioneer period as an ophthalmologist in Tromsø].

Birger Malling (1884-1989) was professor of ophthalmology at the University of Oslo from 1939 to 1954. He spent his first and very active years as a practicing ophthalmologist in Tromsø from 1913 to 1922. Based on interviews, patient journals, notes and publications, this article presents interesting and entertaining fragments of this pioneer period north of the Polar Circle. Malling regarded reconstructive surgery performed by himself on a severely multilated Lapp woman as one of his greatest triumphs. In a lecture in 1921 Malling described a characteristic membrane on the anterior surface of the lens in the pupillary field in glaucomatous eyes. He wrote to Alfred Vogt (1879-1943) in Zürich about his findings, but never received a reply. Vogt later published this finding as his own discovery, with no reference to Malling.

Eye Diseases↗
PubMed1990

Effects of insulin on mononuclear leukocyte beta-adrenoceptor density and adenylate cyclase coupling.

The effects of insulin on human beta-adrenoceptor density and isoproterenol-induced cyclic AMP (cAMP) accumulation were characterized in mononuclear leukocytes from healthy subjects. In cells equilibrated with theophylline (4 mM) at 37 degrees C, insulin (4 microU/ml) was present in periods from 1 to 35 min prior to stimulation. The basal cAMP levels were not influenced. After 1 min pretreatment with insulin, the (-)-isoproterenol concentration necessary to cause half-maximal stimulation (EC50) decreased from 260 to 170 nM (P less than 0.025) and the maximal (-)-isoproterenol response above basal increased from 44 to 63 pmol/10(6) cells (P less than 0.01). The short exposure to insulin caused an increase in the number of functional beta-adrenoceptors from 1420 to 2160 receptors/cell (P less than 0.01). The increased (-)-isoproterenol responsiveness showed a time-dependent decline. When insulin had been present for 35 min before stimulation, the EC50 value had increased to 600 nM (P less than 0.01 vs. control) and the maximal (-)-isoproterenol response above basal was reduced to 29 pmol/10(6) cells (P less than 0.01 vs. control). The receptor density decreased to the pretreatment value (1480 receptors/cell) after 35 min exposure to insulin. The present study shows that insulin modifies the beta-adrenoceptor density as well as the beta-adrenoceptor coupling to adenylate cyclase, dependent on the duration of exposure.

Adenylyl Cyclases↗
PubMed1989

[Alcohol and head injuries].

42 patients with epidural haematoma were operated upon in the surgical department of the regional hospital, Tromsø, in the years 1967-1985. Clinical evaluation showed that 17 of these patients (40.5%) were intoxicated by alcohol at the time of trauma. 14 of the intoxicated (82.4%) but only 7 (28%) of the sober patients, had been injured either in the evening or at night. 13 in the intoxicated group (76.5%) and 10 in the sober group (40%) were hurt by falling or as a result of violence. 15 of the sober group (60%) and 4 intoxicated patients (23.5%) arrived less than 4 hours after the accident. We found a significant difference between the two groups as regards the time lag between accident and arrival at Tromsø hospital.

Adolescent↗
PubMed1989

Double-blind study of naproxen vs placebo in the treatment of acute migraine attacks.

Naproxen was compared with placebo in a double-blind, crossover trial in classic and common migraine. The trial was terminated at a fixed date; 37 patients had entered, 5 of whom were excluded. Naproxen was given as 750 mg at the first symptom of the attack, a total of 1250 mg per 24 h was allowed. Patients were followed for six attacks or three months in each phase, whichever came first. The severity of the headache was significantly less with naproxen in the first 2 h of the attack (p = 0.047), whereas there was no difference when the whole attack was considered. Significantly more patients preferred naproxen (p = 0.042). Side effects occurred in five patients, causing withdrawal of one patient while on naproxen.

Acute Disease↗
PubMed1989

[Illustrations in medical education].

Two different anatomical illustrations of the shoulder were shown to two groups of students, in order to see what they had absorbed. Both figures were of the dorsal aspect of the shoulder. One figure (A) was from a current anatomical atlas, containing abundant details. The other (B) was a schematic drawing including scapula, humerus and three of the dorsal muscles. Altogether 111 medical and physiotherapy students participated in the study. Half of the students were shown Figure A, and the other half Figure B. Both figures were shown for ten seconds. Only 58 per cent of the students that were shown Figure A knew correctly what they had seen, in contrast to those that had seen Figure B where 88 per cent were correct. There is a difference with p less than 0.001. It seems justified to conclude that simple, schematic drawings emphasizing the important points are better for orientation and recollection than the more correct, but also more detailed type of figures.

Anatomy, Artistic↗